• Hemostasis / Coagulation

  What to do when faced with a decrease in PT in children

  Posted by Web master on March 9, 2025 at 10:25 PM

  Analysis of the result of the TP
  [1) The following emergency situations should be identified
  The severity of hepatic injury or coagulation defect is generally proportional to the decrease in PT. The 50% threshold is generally accepted as requiring the opinion of a specialized emergency centre. However, the severity of the pathologies explored by the PT remains essentially clinical, with signs of hepatic encephalopathy for liver damage, or hemorrhagic signs for hemostasis abnormalities.
  [2] False TP decreased
  In order to guarantee a reliable result, the collection tube must be completely filled, gently shaken after collection to avoid the formation of a clot, and transported quickly to the laboratory. In the event of sampling from a venous line, care must be taken that the sample is not contaminated by an infusion solution or an anticoagulant drug. The PT measurement is also disturbed in the event of a particularly high hematocrit (> 55%).
  Apart from these situations, any decrease in PT < 70% must be explored and/or rechecked.
  Lack of synthesis of one or more coagulation factors
  [3) Early vitamin K deficiency
  In early vitamin K deficiency, factor VII is the first to decline because its half-life is the shortest of the vitamin K-dependent factors (6 hours).
  [4) Rare genetic deficiencies
  Most of these rare genetic deficiencies in coagulation factor(s) are of autosomal recessive transmission. Only the severe forms of these pathologies, resulting from bi-allelic alterations, are at risk of hemorrhage. A family study is essential. Hemorrhagic signs may include bleeding on cord fall, intracranial hemorrhages, hematomas and hemarthroses secondary to sometimes minor trauma, or even occurring spontaneously.
  A decrease in all vitamin K-dependent factors (II, VII, IX, X), with normal V and fibrinogen, can correspond to one of the following 3 situations.
  [5] Treatment with vitamin K antagonist
  Treatments with vitamin K antagonists (AVK) lead to a reduction in TP. For the adaptation of AVK treatment doses, it is necessary to use the international normalized ratio (INR) which corresponds to a normalized (standardized) value of the TP. A special case is the accidental consumption of rat poison anticoagulants with VKA properties: this hypothesis must therefore be raised in the event of a decrease in vitamin K-dependent factors without a found cause.
  [6) Newborn case
  Due to hepatic immaturity, the haemostatic balance of the newborn is physiologically different from that of older children and adults. It is therefore essential to interpret the coagulation status of a newborn using age-appropriate standards. In newborns, the levels of vitamin K-dependent factors (II, VII, IX and X) may be reduced compared to adult norms. This phenomenon is even more marked in the case of prematurity. The PT of the healthy newborn is usually normal, unlike the APTT which is frequently elongated. Besides these physiological variations in coagulation, hemorrhagic disease of the newborn is rare but can be extremely serious because it is associated with intracranial, hepatic or adrenal bleeding. It is secondary to a defect in the hepatic synthesis of vitamin K-dependent factors. This pathology is favored by exclusive breastfeeding and prolonged use of antibiotics. The hepatic store of vitamin K at birth is very low. The prevention of hemorrhagic disease of the newborn is based on the systematic administration of vitamin K1 in all newborns from birth. The scheme currently recommended by the French Society of Neonatology for full-term newborns is the oral administration of 3 doses of 2 mg of vitamin K: at birth, on leaving the maternity ward and 1 month after birth (last dose optional under artificial feeding).
  [7] Vitamin K deficiency due to lack of absorption (cholestasis)
  Bile acids are necessary for the absorption of fats including fat-soluble vitamins (A, D, E and K). As a result, cholestasis will induce a decrease in the absorption of vitamin K. The stocks of the latter being low, this will quickly induce a vitamin K deficiency and a defect in the synthesis of factors II, VII, IX and X. with a risk of hemorrhage, particularly intracranial (subdural hematoma). Clinical signs suggestive of cholestasis are jaundice and discolored stools. At the biological level, we observe an elevation of conjugated bilirubin and in the majority of cases of gammaglutamyltransferase (GGT) (except, for example, in progressive familial intrahepatic cholestasis or defects in the synthesis of bile acids).
  res). Infants with early onset cholestasis are particularly at risk due to low vitamin K stores at birth. In case of icteric cholestasis, vitamin K supplementation should be done intravenously at a dose of 10 mg (or intramuscularly if the venous route is impossible). The causes of cholestasis are detailed in the Step by Step “Jaundice in infants” and “Jaundice in older children”
  [8) Hepatocellular insufficiency: decrease in all cofactors
  The liver synthesizes 15% of the body’s proteins. Hepatocellular insufficiency will lead to a drop in PT due to a lack of synthesis of coagulation factors. In this case, a decrease in all the factors is observed in the order of their half-life (factor VII first due to its short half-life and factor V last). The decrease in PT and factor V does not always perfectly reflect the degree of hepatocellular insufficiency, especially when the vitamin K-dependent factors are dissociated (normal), and sometimes overestimates it, as in situations of portal hypertension with hypersplenism. Hepatocellular insufficiency can occur in a previously healthy liver (eg, paracetamol intoxication) or in a liver with cirrhosis (eg, in cholestatic disease). In the case of underlying hepatic pathology, several hepatic causes of lowering of PT can be associated: hepatocellular insufficiency, cholestasis and sometimes consumption in splenomegaly on hypersplenism. The causes of hepatocellular insufficiency are partly detailed in the “Acute hepatitis” Footsteps.
  Consumption or neutralization of one or more coagulation factors
  [9) Disseminated intravascular coagulation
  Disseminated intravascular coagulation (DIC) can lead to both hemorrhagic and thrombotic signs. This state is also accompanied by an increase in fibrin degradation products (FDP), in particular D-dimers. The main etiologies of DIC are sepsis, trauma and other extensive tissue damage, and malignancy. In infants, two additional specific etiologies should be mentioned: on the one hand the homozygous deficiency in proteins C or S resulting in a picture of neonatal aseptic purpura fulminans, and on the other hand the Kasabach-Merritt syndrome, in which a Vascular tumor (kaposiform hemangioendothelioma) is responsible for localized DIC with often severe thrombocytopenia and consumptive coagulopathy.
  [10] Circulating anticoagulant
  Among the causes of decreased PT due to the presence of an acquired circulating anticoagulant, hypoprothrombinemia (decrease in factor II) should be known because it can be responsible for serious bleeding complications. Hypoprothrombinemia is here due to the presence of a specific anti-FII inhibitor (antibody). This table is associated with a decrease in the TP and an elongation of the APTT. These anomalies are not corrected by the mixture test (mixture by the laboratory of the patient’s plasma with a control plasma, then control of the PT/APTT). This picture is usually transient (post-infectious) in children. The follow-up is mainly clinical but a control of the normalization of the coagulation assessment at 6 weeks is justified. This entity must be clearly distinguished from that of circulating anticoagulants of the lupus type in children, associated with an isolated elongation of the APTT with assay of normal coagulation factors. This last entity constitutes, when discovered in an asymptomatic child, a transient, post-infectious anomaly, devoid of thrombotic or hemorrhagic risk and not requiring systematic biological control.
  Conclusion
  The interpretation of a decrease in PT requires taking into account clinical parameters and a certain number of other complementary examinations (mainly APTT, fibrinogen, liver function tests and PT cofactors). The main etiologies of a decrease in PT are vitamin K deficiency due to lack of absorption in the event of cholestasis, hepatocellular insufficiency, treatment with AVK, DIC, and the presence of a circulating anticoagulant.

  ■ Bibliography

  P. Saultier1,2,*, A. Fabre3,4
  1APHM, Hôpital d’Enfants de la Timone, Service d’hématologie, immunologie et oncologie pédiatrique,
  Marseille, France
  2Aix-Marseille Univ, INSERM, INRAe, C2VN, Marseille, France
  3APHM, Hôpital d’Enfants de la Timone, Service de pédiatrie multidisciplinaire, Marseille, France
  4Aix-Marseille Univ, INSERM, MMG, Marseille, France

  

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